Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/5553
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dc.contributor.authorScorza, Fulvio Alexandre [UNIFESP]
dc.contributor.authorSchmitt, Andrea
dc.contributor.authorCysneiros, Roberta Monterazzo [UNIFESP]
dc.contributor.authorArida, Ricardo Mario [UNIFESP]
dc.contributor.authorCavalheiro, Esper Abrão [UNIFESP]
dc.contributor.authorGattaz, Wagner F.
dc.date.accessioned2015-06-14T13:41:29Z
dc.date.available2015-06-14T13:41:29Z
dc.date.issued2010-01-01
dc.identifierhttp://dx.doi.org/10.1590/S1807-59322010000500012
dc.identifier.citationClinics. Faculdade de Medicina / USP, v. 65, n. 5, p. 539-546, 2010.
dc.identifier.issn1807-5932
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/5553
dc.description.abstractPatients with schizophrenia have a two- to three-fold increased risk of premature death as compared to patients without this disease. It has been established that patients with schizophrenia are at a high risk of developing cardiovascular disease. Moreover, an important issue that has not yet been explored is a possible existence of a cerebral focus that could trigger sudden cardiac death in patients with schizophrenia. Along these lines, several structural and functional alterations in the thalamic complex are evident in patients with schizophrenia and have been correlated with the symptoms manifested by these patients. With regard to abnormalities on the cellular and molecular level, previous studies have shown that schizophrenic patients have fewer neuronal projections from the thalamus to the prefrontal cortex as well as a reduced number of neurons, a reduced volume of either the entire thalamus or its subnuclei, and abnormal glutamate signaling. According to the glutamate hypothesis of schizophrenia, hypofunctional corticostriatal and striatothalamic projections are directly involved in the pathophysiology of the disease. Animal and post-mortem studies have provided a large amount of evidence that links the sudden unexpected death in epilepsy (SUDEP) that occurs in patients with schizophrenia and epilepsy to thalamic changes. Based on the results of these prior studies, it is clear that further research regarding the relationship between the thalamus and sudden cardiac death is of vital importance.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFAEPA
dc.format.extent539-546
dc.language.isoeng
dc.publisherFaculdade de Medicina / USP
dc.relation.ispartofClinics
dc.rightsAcesso aberto
dc.subjectBrainen
dc.subjectHearten
dc.subjectSchizophreniaen
dc.subjectSudden cardiac deathen
dc.subjectThalamusen
dc.titleThalamic nuclear abnormalities as a contributory factor in sudden cardiac deaths among patients with schizophreniaen
dc.typeArtigo
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversity of Goettingen Department of Psychiatry
dc.contributor.institutionUniversidade Presbiteriana Mackenzie Centro de Ciências Biológicas e da Saúde Programa de Pós-Graduação em Distúrbios do Desenvolvimento
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.description.affiliationUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniversity of Goettingen Department of Psychiatry
dc.description.affiliationUniversidade Presbiteriana Mackenzie Centro de Ciências Biológicas e da Saúde Programa de Pós-Graduação em Distúrbios do Desenvolvimento
dc.description.affiliationUniversidade Federal de São Paulo (UNIFESP) Departamento de Fisiologia
dc.description.affiliationUniversidade de São Paulo Faculdade de Medicina de Ribeirão Preto Departamento de Neurociências e Ciências do Comportamento
dc.description.affiliationUniversidade de São Paulo Faculdade de Medicina Instituto de Psiquiatria
dc.description.affiliationUnifespUNIFESP, Depto. de Fisiologia
dc.identifier.fileS1807-59322010000500012.pdf
dc.identifier.scieloS1807-59322010000500012
dc.identifier.doi10.1590/S1807-59322010000500012
dc.description.sourceSciELO
dc.identifier.wosWOS:000278959900012
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